We have established that one molecular form of gastrin, G17, is the principal hormonal regulator of the chemical phase of gastric acid secretion in man and that patients with duodenal ulcer are more sensitive to their own endogenously released gastrin than normal subjects. One subgroup of ulcer patients was identified who released an inappropriate amount of gastrin compared with the amount required to produce half-maximal gastric acid secretion. We will attempt to define this subgroup further by studying the gastrin release and gastric acid secretory response to small intravenous doses of bembesin, a potent gastrin releasing agent. In addition we will try to identify abnormalities in mechanisms that normally inhibit the release of gastrin, such as the cholinergic inhibitory mechanism and gastric somatostatin.